BackgroundApical Periodontitis (AP) is an inflammatory disease that affects the tissues surrounding the root end of a tooth. The disease which is caused by endodontic infections presents in different clinical ways including development of an acute abscess. Recent studies have provided information suggesting role of a multitude of factors in pathogenesis of acute apical abscess (AAA). In this case-control study, our goal was to evaluate the frequency and potential role of two common polymorphisms of toll like receptor-4 (TLR-4) gene; Thr399Ile (1196 C>T) and Asp299Gly (+896 A>G), in 50 patients with AAA as cases and 50 patients with asymptomatic apical periodontitis (AAP) as controls.Material and MethodsSaliva sample containing mucosal epithelial cells was used for DNA extraction. Polymorphisms were detected by Tetra-ARMS (Amplification Refractory Mutation System) PCR method. Statistical analyses were carried out in SPSS 21 software.ResultsHomozygous wild type (CC) and heterozygous (CT) genotypes of Thr399Ile polymorphism were detected in 84% and 16% of AAA patients respectively. In controls, respective ratios were 94% (CC) and 6% (CT). Observed difference was not statistically significant (P>0.05) for distribution of these genotypes. The mutant homozygous (TT) genotype of this polymorphism was identified in neither of the participants. Overall, T allele frequency was obtained 8% in AAA and 3% in AAP (OR=2.6, 95% CI; 0. 6-10.6, p>0.05). For Asp299Gly polymorphism, no individual was detected with the mutant allele in case or control groups.ConclusionsOur results indicated a possible role for Thr399Ile polymorphism in acute presentations of abscess in AAA. However, the impact of this polymorphism needs to be more assessed in future studies. Key words:Genetic polymorphism, periapical abscess, periapical periodontitis, toll-like receptor 4.

Abstract. Type-2 diabetes (T2D) is a multifactorial (environmental and genetic factors) and global epidemic disease with an estimated high prevalence worldwide. Studies have indicated that nitric oxide synthase 3 (NOS3) has several important roles in the pathogenesis of T2D. The present study aims to investigate the association between NOS3 rs1800779(A/G) and T2D in an Iranian sample population. A case-control study was conducted on 250 T2D patients and 250 healthy control subjects (HCs). Genotyping of the rs1800779(A/G) variant was conducted using a Tetra-Amplification Refractory Mutation System polymerase chain reaction. The frequencies of genotypes AA, AG and GG polymorphisms were 56.8, 39.2 and 4% in the T2D group, and 42.8, 56 and 1.2% in the HCs group, respectively. The frequency of the minor (G) allele was 23.6% in the T2D group and 29.2% in the HCs group. The genotype frequencies of the rs1800779(A/G) variant demonstrated statistically significant differences between T2D and controls in a codominant model (AG vs. AA, OR=0.527, 95% CI=0.368-0.756, P<0.001) and dominant model (AG+GG vs. AA, OR=0.569, P=0.002). There was no significant association between clinical and demographic characteristics and the NOS3 rs1800779(A/G) polymorphism in dominant status (P>0.05). The dominant model and AG genotype of NOS3 rs1800779(A/G) polymorphism may had a protective effect on T2D of Iranian population.